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Biomedical subjects

A Verheyen

Publications and source records attributed to A Verheyen.

At least 37 records · Page 2Linked to original sources

Localization of calcium in skeletal and cardiac muscle.

The requirement of calcium (Ca2+) in the excitation-contraction coupling of both skeletal and cardiac muscle is well established. However, the exact location of the intracellular storage sites of Ca2+ is not firmly established. We report here on the ultrastructural ultrastructural distribution of Ca2+ in white and red skeletal muscle and in cardiac muscle of the rat using combined phosphate-pyroantimonate (PPA) and oxalate-pyroantimonate (OPA) procedures. The methods are based on (a) stabilization and/or trapping of Ca2+ during the primary fixation step in glutaraldehyde by potassium phosphate or oxalate; (b) subsequent wash-out of all non-trapped cations such as Na+ and Mg2+ in potassium phosphate or oxalate; (c) conversion of the complexed or trapped Ca2+ into an electron-dense calcium pyroantimonate salt in 100 micron-thick tissue sections; and (d) wash-out of the excess potassium pyroantimonate at alkaline pH. With the OPA procedure, mitochondria of all muscle types showed little precipitate. The junctional sarcoplasmic reticulum was strongly reactive in relaxed white skeletal muscle, negative in contracted white fibres and negative in red skeletal and cardiac muscle, independent of the state of relaxation-contraction. Other organelles were essentially free of deposits. With the PPA method, the precipitate was almost exclusively confined to the sarcolemma and its T-tubular invaginations in cardiac and slow skeletal muscle, and was absent in fast skeletal muscle. Apart from occasional deposits in mitochondria, all other organelles were free of muscle. Apart from occasional deposits in mitochondria, all other organelles were free of precipitate. The sarcolemma-associated deposits were clearly confined to the inner leaflet of the lipid bilayer. The amount of precipitate varied within the contraction cycle, relaxed cells possessing the highest density. Exposure of the tissue to La3+ resulted in the complete absence of sarcolemma-bound precipitate suggesting that the Ca2+ is exchangeable. Furthermore, these cytological data suggest a basic difference in Ca2+ storage between white skeletal muscle on the one hand, and red skeletal and cardiac muscle on the other.

Animals↗

Influence of vitamin C on the metabolism of arachidonic acid and the development of aortic lesions during experimental atherosclerosis in rabbits.

Feeding rabbits a cholesterol-rich diet (0.3%) resulted in morphological changes and a decrease in the prostacyclin production by the aortic endothelium. Addition of vitamin C (0.1%) to the cholesterol-rich diet resulted in a decreased lipid infiltration and intimal thickening. Although there was a tendency to restore the prostacyclin output, vitamin C, in the amount administered, was unable to completely normalise the endothelial PGI2 production.

Animals↗

Serotonin-induced blood flow changes in the rat hindlegs after unilateral ligation of the femoral artery. Inhibition by the S2 receptor antagonist ketanserin.

Collateral arteries can clearly be visualized in corrosion cast material after ligation of the femoral artery in rats. To characterize the influence of serotonin on the blood circulation under the experimental condition of unilateral ligation, we performed intermuscular thermoflow measurements. The data showed that intraperitoneal serotonin (8.7 and 20 mg.kg-1) injection markedly reduced the muscle temperature in both hindlegs. However, the effect was significantly more pronounced on the ligated side, where the blood was supplied through a collateral circulation, than on the non-ligated side with its normal arterial vasculature. Almost identical changes were obtained in rats with an early as well as in animals with a more advanced stage of collateral development (challenge with 8.7 mg.kg-1 serotonin). Evans blue dye experiments and angiographic data further revealed that, after challenge with 20 mg.kg-1 serotonin, the severe temperature decrease at the ligated side probably reflected a nearly complete blockage of blood supply. Pretreatment with the S2 receptor antagonist ketanserin (2.5 mg.kg-1) resulted in a significant reduction in the extent and duration of the serotonin-induced temperature decrease as revealed by the temperature measurements; such a treatment inhibited also the blockage in blood flow as seen with the other techniques. This study shows that serotonin, through its vasoconstrictive properties, can restrict the blood flow to the lower extremities of the rat, particularly when the blood is supplied through collateral circulation. This probably results in moderate to severe skeletal muscle ischaemia. It also suggests that the vasoconstriction is not only important in the inhibition of collateral blood flow in recently established collaterals but also in collateral vessels in a more advanced stage of development. The in vivo vasoconstriction and subsequent reduction of the blood supply caused by serotonin can be effectively counteracted by pretreatment with ketanserin.

Angiography↗

Echinococcus granulosus: the influence of mebendazole therapy on the ultrastructural morphology of the germinal layer of hydatid cysts in humans and mice.

Upon ultrastructural examination it was found that prolonged mebendazole therapy of patients with hydatid disease often resulted in complete necrosis of the germinal layer of Echinococcus granulosus cysts. The affected cysts showed only remnants of degenerated germinal layer tissue including heterogeneous vesicular membranes, electron-dense amorphous structures, myeloid bodies, lipid globules, crystal-like precipitates and remnants derived from muscular tissue. Examination of the hydatid cysts of treated mice revealed the same time-related deteriorative effect of the anthelmintic as described previously for other cestode species. The advanced stage of degeneration of the germinal layer tissue observed in the murine cysts after treatment resembled the morphologic features present in the necrotic human cysts and gave additional information about the degeneration phenomenon.

Animals↗

The effect of mebendazole on sheep hydatid cysts as demonstrated by electron microscopy.

The ultrastructural changes induced in hydatid cysts from lungs of sheep after medication with one or two courses of mebendazole (Ovitelmin), each lasting 3 wk, are described. The hydatid germinal membrane tissue collected from the treated sheep showed complete degeneration of the tegumental and subtegumental structures and minor degree of calcification. Lung hydatid cysts of the untreated sheep presented normal ultrastructural configurations.

Animals↗

Scanning electron microscopic observations of Cysticercus fasciolaris (=Taenia taeniaeformis) after treatment of mice with mebendazole.

The time-related topographical changes in mature cysticerci of Taenia taeniaformis induced after medication of infected mice with 250 ppm of mebendazole are described. The changes included the gradual disappearance of microtriches and progressive degeneration of the tegment resulting in an irregular surface with grooves, holes, and craterlike structures. Host cells adhered to the altered areas and the number of these cells increased when more severe changes became apparent. Finally the necrotized cysticerci, which lost their tegument completely, were almost entirely covered with adhesive host cells. A difference in the time sequence of the reported changes occurred between the scolex, the pseudoproglottids, and the bladder. This difference in susceptibility towards the drug between the three parts of the parasite in relation to the morphology of their microtrichous covering is discussed.

Animals↗

Effects of levamisole on the ultrastructure of mitochondria in the liver of Beagle dogs.

Purebred Beagle dogs were treated daily for 6 days with levamisole in oral doses of 10 mg/kg body weight. Liver biopsies taken before and after treatment showed no ultrastructural differences. Intramitochondrial paracrystalline inclusions before, as well as after, the drug administration were rare. Other minor abnormalities, in a few mitochondria, were as frequent before as after the drug treatment.

Animals↗

Activated reptilase clot retraction of dog platelet-rich plasma: differences with human platelet-rich plasma.

The retraction of dog platelet-rich plasma (PRP) clotted with Reptilase in the presence of inducers and inhibitors of the platelet adhesion-aggregation reaction was studied. In contrast to human cells, dog platelets fail to support retraction in an ADP-Reptilase system. With Thrombofax as aggregation inducer, slight (without additional CaCl2-MgCl2) to moderate (with additional CaCl2-MgCl2) retraction occurs. In contrast to human samples, such retraction is inhibited by platelet release inhibitors. Electron-microscopic examinations show that Thrombofax, but not ADP, induces the formation of large cytoplasmic protrusions from dog platelets. Such formation is inhibited by release-inhibitors. The results of the study support the concept that platelet pseudopod formation, rather than the release reaction, is a prerequisite for clot retraction.

Adenosine Diphosphate↗

Morphological changes in cysticerci of Taenia taeniaeformis after mebendazole treatment.

The progressive micromorphological changes in Taenia taeniaeformis cysticerci, induced by a single parenteral treatment of the infected mice with mebendazole, are described. The time-related alterations concerned the tegument and tegumental cells and were successively: disappearance of microtubules, accumulation of secretory substances in the Golgi areas, decrease in number to complete loss of microtriches, "ballooning" of all tegumental cells with subsequent burst, vacuolization and degeneration of the tegument, and finally necrosis of the pseudoproglottids. Similar but less pronounced injuries were seen in the scolices, although microtubules disappeared as early as in the pseudoproglottids. Microtubules from the host tissues remained intact. The meaning of the apparent primary interference of mebendazole with the microtubular system in relation to the subsequently observed death of the cysticercoids is discussed.

Animals↗